DESCRIPTION:(From the Abstract) Lesions of the cerebral cortex sustained early in life provoke system wide repercussions that include substantial rewiring of remaining subcortical and cortical pathways. These repercussions contribute significantly to functional compensations by subcortical and cortical neurons and to the sparing of perceptual and cognitive processes that are profoundly impaired following equivalent damage incurred by the mature brain. The long- term goal of the proposed work is to identify the classes of functions that are spared by the early cortical damage, and to identify the neural basis of the sparing. The specific aim of the proposed work is to apply a battery of tasks to extend our knowledge of the neural functions spared by early lesions of areas 17 and 18 and to investigate the contributions middle suprasylvian (MS) and the ventral part of the posterior suprasylvian (vPS) regions of extrastriate cortex make to the sparing. Studies will be carried out on cats which incurred damage to areas 17 & 18 on the day of birth or at one month of age, and comparison data will be collected from intact cats and cats which incurred equivalent damage in adulthood. They will train cats, when mature, on a battery of behavioral tasks for functions normally associated with: 1) damaged areas 17 & 18, 2) MS and vPS extrastriate regions, and 3) afferent alpha (Y) or beta (X) signal transfer streams, and determine the cats' visual capacities. They will then implant cooling probes and reversibly deactivate MS and vPS cortices bilaterally, and in turn, test the contributions the two regions make to the spared behaviors. The behavioral tasks and comparisons between groups will reveal 1) the classes of tasks that are spared following the early lesions of areas 17 and 18; 2) age dependent differences in spared functions; 3) whether the remaining regions of cortex are able to adopt functions normally associated with the damaged areas 17 & 18; and 4) whether functions normally associated with a discrete cortical region remain localized following the early lesion or whether they become dispersed, as the substantial rewiring of extrastriate pathways suggest. On all cats they will carry out periodic assessments to verify the constancy of behaviors and cooling-induced defects across test sessions. At the end of testing they will verify cooling deactivation of neurons, assess the extent of cortex deactivated by cooling, and determine amount of areas 17 & 18 removed. The proposed work will provide detailed information on the capacities of the immature cerebral cortex to compensate for perceptual and cognitive functions lost or handicapped following equivalent damage of the mature cerebrum. The identification of these capacities is important for steering future anatomical, physiological and behavioral efforts directed at comprehending the consequences of early cerebral cortical damage, and for developing therapeutic strategies that attempt to enhance the sparing of cortical functions.